RESUMO
OBJECTIVES: It is uncertain whether eradication of Helicobacter pylori--without a prolonged suppression of acid secretion--is sufficient to allow healing of peptic ulcers. We evaluated whether eradication of H. pylori with no following anti-secretory medication then administered is sufficient for treatment of peptic ulcers. We also looked at the impact of non-steroidal anti-inflammatory drug (NSAID) and acetylsalicylic acid (ASA) use on ulcer relapses. METHODS: The effect of eradication on ulcer healing and relapse rate was analysed in 115 patients, randomly allocated to four treatment groups: (1) quadruple therapy (28); (2) dual therapy (n-30); (3) triple therapy (n=27); and (4) lansoprazole and placebo (n=30). Endoscopic assessment was performed at 0, 8, and 52 weeks. RESULTS: The ulcer healing rate was 100% [95% confidence interval (CI), 95-100%] in H. pylori-negative and 83% (95% CI, 67-94%) in H. pylori-positive patients (P<0.01). In patients who used NSAIDS or ASA, the healing rates was 100% (95% CI, 73-100%) and 75% (95% CI, 19-99%) in H. pylori-negative (12 patients) and H. pylori-positive patients (four patients) (P = not significant). Ulcer relapses occurred in 5% (95% CI, 1-13%) of H. pylori-negative and in 36% (95% CI, 19-56%) of H. pylori-positive patients (P < 0.01). In H. pylori-negative patients who used NSAIDs or ASA the ulcer relapse rate was 30% (95% CI, 7-65%), whereas the ulcer relapse rate was 2% (95% CI, 0.4-10%) in patients who did not use NSAIDs or ASA (P < 0.05). No difference in ulcer relapse rate in H. pylori-positive patients who used or did not use NSAIDs or ASA was found. The eradication rate of H. pylori was 93% (95% CI, 76-99%) in the quadruple therapy group, 83% (95% CI, 64-94%) in the dual therapy group, 100% (95% CI, 87-100%) in the triple therapy group, and 0% (95% CI, 0-12%) in the lansoprazole and placebo group. CONCLUSIONS: Eradication treatment for H. pylori-positive gastric or duodenal ulcer is sufficient, with no need to follow it with anti-secretory medication. Cure of the infection reduces ulcer relapses in patients who did not use NSAIDs or ASA.
Assuntos
Antibacterianos , Quimioterapia Combinada/uso terapêutico , Úlcera Duodenal/microbiologia , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori , Omeprazol/análogos & derivados , Úlcera Gástrica/microbiologia , 2-Piridinilmetilsulfinilbenzimidazóis , Adulto , Idoso , Anti-Inflamatórios não Esteroides/uso terapêutico , Antiulcerosos/uso terapêutico , Aspirina/uso terapêutico , Úlcera Duodenal/tratamento farmacológico , Úlcera Duodenal/patologia , Feminino , Gastrite/tratamento farmacológico , Gastrite/microbiologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Humanos , Lansoprazol , Masculino , Pessoa de Meia-Idade , Omeprazol/uso terapêutico , Estudos Prospectivos , Inibidores da Bomba de Prótons , Recidiva , Úlcera Gástrica/tratamento farmacológico , Úlcera Gástrica/patologia , Resultado do TratamentoAssuntos
Hepatite Viral Humana/patologia , Cirrose Hepática/patologia , Doença Aguda , Biópsia por Agulha , Doença Crônica , Progressão da Doença , Feminino , Seguimentos , Hepatite Viral Humana/complicações , Humanos , Imuno-Histoquímica , Cirrose Hepática/etiologia , Masculino , Índice de Gravidade de DoençaRESUMO
AIM: To study the association between helicobacters and chronic liver diseases and chronic inflammatory bowel diseases. PATIENTS AND METHODS: Thirty-two patients with various chronic liver diseases and 137 patients with inflammatory bowel disease were enrolled. Antibodies to H. pylori, H. hepaticus, H. bilis, and H. pullorum were measured by enzyme immunoassay (EIA), and sera positive in a non-pylori helicobacter EIA were further examined by immunoblot assay. Detection of Helicobacter DNA in liver biopsies was done by denaturating gradient gel electrophoresis of PCR products (PCR-DGGE) and DNA sequence analysis. RESULTS: Six inflammatory bowel disease patients, four with ulcerative colitis and two with Crohn's disease, and one liver disease patient with autoimmune cholangitis had antibodies to non-pylori helicobacters by an immunoblot assay. Four immunoblot assay-negative patients, three with autoimmune and one with non-autoimmune liver disease, had Helicobacter DNA in liver biopsies; three of the polymerase chain reaction (PCR) products were closely related to non-pylori helicobacters. CONCLUSION: Evidence for non-pylori helicobacters was scant in Finnish patients with inflammatory bowel disease or chronic but not end stage liver disease. We cannot, however, rule out their role in these diseases.
Assuntos
Infecções por Helicobacter/diagnóstico , Helicobacter/isolamento & purificação , Doenças Inflamatórias Intestinais/diagnóstico , Doenças Inflamatórias Intestinais/microbiologia , Hepatopatias/diagnóstico , Hepatopatias/microbiologia , Adulto , Idoso , Doença Crônica , DNA Bacteriano/metabolismo , Feminino , Infecções por Helicobacter/complicações , Infecções por Helicobacter/metabolismo , Humanos , Doenças Inflamatórias Intestinais/sangue , Fígado/metabolismo , Fígado/patologia , Hepatopatias/metabolismo , Masculino , Pessoa de Meia-Idade , Desnaturação de Ácido Nucleico , Reação em Cadeia da PolimeraseRESUMO
OBJECTIVE: A causal relationship between Helicobacter pylori (H. pylori) and peptic ulcer complications remains obscure. The aim of this study was to determine the importance of H. pylori and other risk factors for healing rate, ulcer recurrence, and rebleeding in patients with bleeding peptic ulcer. METHOD: A total of 223 patients with H. pylori positive bleeding peptic ulcer were randomly allocated to three treatment groups: 1) quadruple therapy (QT) (88 patients); 2) dual therapy (DT) (88 patients); and 3) omeprazole and placebo therapy (OPl) (47 patients). Endoscopic assessment was performed initially and at 8 and 52 wk. Ulcer healing and eradication rates were assessed; endpoints were ulcer relapse and ulcer rebleeding during 52 wk. RESULTS: Results after 8 and 52 wk were available for 211 and 179 patients, respectively. Eradication rate was 100% (95% CI = 96-100%) in the QT, 84% (95% CI = 74-91%) in the DT, and 4% (95% CI = 1-15%) in the OPl group. Ulcer healing rate was 95% (95% CI = 91-98%) in H. pylori negative and 8% (95% CI = 70-91%) in H. pylori positive patients. Ulcer relapses occurred in 2% (95% CI = 0.5-6%) of H. pylori negative and in 38% (95% CI = 24-54%) of H. pylori positive patients, and rebleeding occurred in five patients (three H. pylori positive and two negative). CONCLUSIONS: Eradication of H. pylori infection enhances healing of bleeding peptic ulcers after endoscopic therapy. H. pylori infection is an important independent risk factor for relapsing of nonbleeding ulcers in patients with bleeding peptic ulcer.